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牛胎盘提取物通过增强肠道屏障、改善免疫功能和恢复肠道微生物群来减轻环磷酰胺诱导的肠道损伤。

Cow Placenta Extract Ameliorates Cyclophosphamide-Induced Intestinal Damage by Enhancing the Intestinal Barrier, Improving Immune Function, and Restoring Intestinal Microbiota.

作者信息

Zhao Yuquan, Zhang Zeru, Tang Anguo, Zeng Zhi, Zheng Weijian, Luo Yuxin, Huang Yixin, Dai Xinyi, Lu Wei, Fan Lei, Shen Liuhong

机构信息

The Key Laboratory of Animal Disease and Human Health of Sichuan Province, The Medical Research Center for Cow Disease, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China.

Party School of the Communist Party of China Yaan Municipal Committee, Yaan 625014, China.

出版信息

Vet Sci. 2024 Oct 14;11(10):505. doi: 10.3390/vetsci11100505.

DOI:10.3390/vetsci11100505
PMID:39453097
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11512425/
Abstract

Immunosuppression undermines intestinal barrier integrity. Cow placenta extract (CPE) primarily consists of active peptides with immunomodulatory and antioxidant effects. This study aimed to examine the preventive effect of CPE against intestinal damage induced by cyclophosphamide (Cy) in immunosuppressed mice. Thirty-six mice were randomly allocated into three groups: control group (C), model group (M), and treatment group (CPE). The mice in the CPE group were provided with 1500 mg/kg/day of CPE via gavage. In the last 3 days, mice in the groups M and CPE received intraperitoneal injections of 80 mg/kg/day of Cy. The results showed that CPE improved intestinal barrier function by decreasing serum d-Lactate (D-LA) levels and diamine oxidase (DAO) activity, while elevating the relative expression of , (), and () mRNA. Additionally, CPE improved the immune organ index and elevated the levels of secretory immunoglobulin A (sIgA), superoxide dismutase (SOD), interleukin-1beta (IL-1β), interleukin-4 (IL-4), interleukin-10 (IL-10), and tumor necrosis factor-α (TNF-α) in the intestine, thereby enhancing intestinal mucosal immune function. Furthermore, CPE improved the diversity of intestinal microbiota and increased the abundance of , , and , which promoted the proper functioning of the intestines. These findings suggest that CPE effectively ameliorates Cy-induced intestinal damage by enhancing the intestinal barrier, improving immune function, and restoring intestinal microbiota.

摘要

免疫抑制会破坏肠道屏障的完整性。牛胎盘提取物(CPE)主要由具有免疫调节和抗氧化作用的活性肽组成。本研究旨在探讨CPE对免疫抑制小鼠中环磷酰胺(Cy)诱导的肠道损伤的预防作用。36只小鼠随机分为三组:对照组(C)、模型组(M)和治疗组(CPE)。CPE组小鼠通过灌胃给予1500 mg/kg/天的CPE。在最后3天,M组和CPE组小鼠腹腔注射80 mg/kg/天的Cy。结果表明,CPE通过降低血清d-乳酸(D-LA)水平和二胺氧化酶(DAO)活性,同时提高紧密连接蛋白1(ZO-1)、闭合蛋白(Occludin)和Claudin-1 mRNA的相对表达,改善了肠道屏障功能。此外,CPE改善了免疫器官指数,提高了肠道中分泌型免疫球蛋白A(sIgA)、超氧化物歧化酶(SOD)、白细胞介素-1β(IL-1β)、白细胞介素-4(IL-4)、白细胞介素-10(IL-10)和肿瘤坏死因子-α(TNF-α)的水平,从而增强了肠道黏膜免疫功能。此外,CPE改善了肠道微生物群的多样性,增加了双歧杆菌属(Bifidobacterium)、乳酸杆菌属(Lactobacillus)和阿克曼菌属(Akkermansia)的丰度,促进了肠道的正常功能。这些发现表明,CPE通过增强肠道屏障、改善免疫功能和恢复肠道微生物群,有效减轻了Cy诱导的肠道损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/b7382243c0e2/vetsci-11-00505-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/877b363fd4d0/vetsci-11-00505-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/ce1b127b1fa2/vetsci-11-00505-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/9416d0591a80/vetsci-11-00505-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/7ea3be453923/vetsci-11-00505-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/8bdf36295fc4/vetsci-11-00505-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/7770bad967be/vetsci-11-00505-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/6f9c35476d9c/vetsci-11-00505-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/7e19a1957e46/vetsci-11-00505-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/b7382243c0e2/vetsci-11-00505-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/877b363fd4d0/vetsci-11-00505-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/ce1b127b1fa2/vetsci-11-00505-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/9416d0591a80/vetsci-11-00505-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/7ea3be453923/vetsci-11-00505-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/8bdf36295fc4/vetsci-11-00505-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/7770bad967be/vetsci-11-00505-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/6f9c35476d9c/vetsci-11-00505-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/7e19a1957e46/vetsci-11-00505-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6047/11512425/b7382243c0e2/vetsci-11-00505-g009.jpg

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